23. What is the difference between intracellular signaling and intercellular signaling?
24. How are the effects of paracrine signaling limited to an area near the signaling cells?
25. What are the differences between internal receptors and cell-surface receptors?
26. Cells grown in the laboratory are mixed with a dye molecule that is unable to pass through the plasma membrane. If a ligand is added to the cells, observations show that the dye enters the cells. What type of receptor did the ligand bind to on the cell surface?
27. Insulin is a hormone that regulates blood sugar by binding to its receptor, insulin receptor tyrosine kinase. How does insulin’s behavior differ from steroid hormone signaling, and what can you infer about its structure?
28. The same second messengers are used in many different cells, but the response to second messengers is different in each cell. How is this possible?
29. What would happen if the intracellular domain of a cell-surface receptor was switched with the domain from another receptor?
30. If a cell developed a mutation in its MAP2K1 gene (encodes the MEK protein) that prevented MEK from being recognized by phosphatases, how would the EGFR signaling cascade and the cell’s behavior change?
31. What is a possible result of a mutation in a kinase that controls a pathway that stimulates cell growth?
32. How does the extracellular matrix control the growth of cells?
33. A scientist notices that a cancer cell line shows high levels of phosphorylated ERK in the absence of EGF. What are two possible explanations for the increase in phosphorylated ERK? Be specific in which proteins are involved.
34. What characteristics make yeasts a good model for learning about signaling in humans?
35. Why is signaling in multicellular organisms more complicated than signaling in single-celled organisms?
36. Pseudomonas infections are very common in hospital settings. Why would it be important for doctors to determine the bacterial load before treating an infected patient?